Coria R, Saviñon-Tejeda A L, Birnbaumer L
Departamento de Microbiología, Universidad Nacional Autónoma de México, México, D.F.
FEBS Lett. 1995 Jun 26;367(2):122-6. doi: 10.1016/0014-5793(95)00526-f.
The yeast pheromone response pathway involves the activation of a heterotrimeric G protein composed by SCG1 (alpha) (also GPA1), STE4 (beta), and STE18 (gamma) subunits by the pheromone-activated receptors STE2 and STE3 in a and alpha cells, respectively. Upon exchange of bound GDP for GTP in the SCG1 subunit, the release of STE4/STE18 dimer occurs which, in turn causes activation of downstream effectors leading growth arrest and mating competence. Over-expression of STE4 also leads to growth arrest in a STE18 dependent manner. Removal of 6 amino acids from the C-terminus of STE4 rendered a subunit incapable of downstream signalling but still able to interact with STE18. This delta C6 mutant acts as a dominant negative because it blocks the growth arresting effect obtained by over-expression of STE4. The inhibitory effect of STE4 delta C6 is dependent on the presence of the SCG1 subunit in a STE2 but not ste2 background. Inhibition of the growth arresting effect of STE4 by the delta C6 mutant is not due to competition at the effector site, but rather involves an intrinsic activity of STE2 that is dependent on SCG1.
酵母信息素应答途径涉及在a细胞和α细胞中，信息素激活的受体STE2和STE3分别激活由SCG1（α）（也称为GPA1）、STE4（β）和STE18（γ）亚基组成的异源三聚体G蛋白。在SCG1亚基中结合的GDP被GTP交换后，STE4/STE18二聚体释放，这反过来又导致下游效应器激活，导致生长停滞和交配能力。STE4的过表达也以STE18依赖的方式导致生长停滞。从STE4的C末端去除6个氨基酸使一个亚基无法进行下游信号传导，但仍能与STE18相互作用。这种δC⁶突变体作为显性负性起作用，因为它阻断了STE4过表达所获得的生长停滞效应。STE4δC⁶的抑制作用取决于STE2背景中SCG1亚基的存在，而不是ste2背景。δC⁶突变体对STE4生长停滞效应的抑制不是由于效应位点的竞争，而是涉及依赖于SCG1的STE2的内在活性。
